Prenatal exposure to manganese and objectively measured sleep disturbances in early childhood.

Inadequate sleep in childhood can impact long-term neurodevelopmental outcomes; thus, identifying modifiable risk factors amenable to intervention is a priority. Development of sleep neuroarchitecture begins in utero. Manganese (Mn) is a trace element known to be both an essential element for optimal neurodevelopment and, at insufficient or excess levels, a neurotoxicant. We examined associations between prenatal urinary Mn levels and objectively measured sleep outcomes in children aged 6.7 ± 2.0 years and explored sex-specific effects. Sleep was assessed using multi-day actigraphy (n = 222) and single-night in-home polysomnography (PSG) (n = 102). Linear and non-linear associations between prenatal log-transformed Mn levels and sleep outcomes were examined using multivariable linear regression and generalized additive models, respectively. Non-linear associations were examined based on low, moderate (referent group) and high Mn levels indexed by tertiles. Sex-specific effects were evaluated using 2-way interaction terms. A doubling increase in Mn was associated with a 30.9 min (95 % CI = -52.0, -9.86) decrease of average sleep period duration and a 21.9 min (95 % CI = -39.9, -4.02) decrease of average sleep duration on actigraphy; associations were more pronounced in males. Compared to children born to mothers with moderate prenatal urinary Mn levels, children whose mothers had "low" Mn had a percent increase in minutes of wake after sleep onset (WASO) (β = 89.6; 95 % CI = 16.2, 206.5) and a decrease in sleep efficiency percentage (β = -6.47; 95 % CI = -11.3, -1.68) on PSG. Sleep problems may be influenced by environmental exposures, such as metals, and disruption can occur as early as pregnancy.